Alzheimer's disease is characterized by the accumulation of amyloid plaques, composed of Aβ proteins, and neurofibrillary tangles, composed of tau proteins. It can be genetically linked to mutations that increase the propensity for Aβ to form pathogenic aggregates; interestingly, however, it is never linked to mutations in tau. An implication of this genetic dichotomy is that the formation of a pathogenic form of Aβ, but not tau, initiates Alzheimer's disease. Aβ*56 (Abeta star 56) has been proposed to be the pathogenic form of Aβ that initiates Alzheimer's disease.
Aβ*56 requires tau to impair memory function. Tau is therefore an Aβ effector molecule. The clinical observation that amyloid plaques deposit prior to abnormal increases in spinal fluid tau is consistent with this idea. These and other related results indicate that the pathogenesis of Alzheimer's disease requires both the Aβ and tau proteins.